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64th Annual Meeting of the German Society of Neurosurgery (DGNC)

German Society of Neurosurgery (DGNC)

26 - 29 May 2013, Düsseldorf

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Spreading depression triggers ictalform activity in disinhibited neuronal tissues

Meeting Abstract

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  • M. Eickhoff - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland
  • S. Kovac - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland
  • P. Shahabi - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland
  • Maryam Khaleghi Ghadiri - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland
  • Walter Stummer - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland
  • Ali Gorji - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Münster, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 64. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Düsseldorf, 26.-29.05.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. DocMO.10.04

doi: 10.3205/13dgnc083, urn:nbn:de:0183-13dgnc0830

Published: May 21, 2013

© 2013 Eickhoff et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.

Outline

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Objective: Spreading depression (SD) belongs to the domain of the pathophysiology of the brain and has been linked to various neurological disorders, including migraine with aura, cerebrovascular diseases, head injury, transient global amnesia, and epilepsy. The close kinship between SD and experimental epileptic activity stimulated extensive investigation into the mutual relationship of these two phenomena. The aim of present study was to investigate the basic cellular mechanism of SD triggering epileptiform potentials (EFP) in partially disinhibited brain slices.

Method: Intracellular recordings were performed in the neocortex, hippocampus and amygdala after perfusion of sub-threshold of GABAA antagonist bicuculline. Induction of SD in combined amygdala-hippocampus-cortex slices pre-treated with sub-threshold concentration of GABAA antagonist bicuculline triggered ictal activities in cortical as well as subcortical brain structures.

Results: Propagation of SD significantly depolarised the membrane, decreased the neuronal membrane input resistance, and threshold potentials. Both the amplitude and duration of action potentials also reduced and the frequency of that enhanced after induction of SD. In addition, propagation of SD decreased the amplitude and duration of after hyperpolarisation.

Conclusions: The data indicate that a partial reduction of inhibitory tone by application of a GABAA antagonist promotes triggering of EFP by SD. This may important in occurrence of seizure attacks in neurological disorders in which brain suffers from partial impairment of inhibitory ton, such as brain ischemia and epilepsy.